Acute gastroenteritis is one of the world's most significant disease problems. An estimated 3 to 5 million people die each year from gastroenteritis, mostly in the developing world (Glass et al., 2001). In the United States, viral gastroenteritis is one of the most common acute illnesses, second only to viral respiratory diseases (Glass et al., 2001). Although several viruses cause gastroenteritis, the most clinically relevant include rotaviruses, caliciviruses, astroviruses, and enteric adenoviruses (Cukor et al., 1984).
Viral gastroenteritis occurs in both an endemic and epidemic fashion, based on the routes of transmission and host response. The most common endemic viruses are group A rotaviruses, enteric adenoviruses, astroviruses and the Sapporo-like viruses (caliciviruses) (Glass et al., 2001). These infections are virtually universal in the first years of life. It is believed that during early childhood, immunity develops to these agents providing protection against recurring infection and explaining the decrease in cases in older children and adults (Kurtz et al., 1978; Kurtz et al., 1979; Mitchell, 2002). Epidemic viruses are best characterized by the Norwalk-like viruses (calicivirus) and the group B rotaviruses. These viruses affect people of all ages, and outbreaks are typically linked to contaminated water and/or food (Goodgame, 2001).
Astroviruses, small round, non-enveloped viruses, typically 28-30 nm in diameter, are implicated in epidemics, usually associated with an institutional setting like a hospital, retirement community, or military base, and they have been isolated from shellfish linked to food borne disease (Matsui et al., 2001). Astroviruses have been reported to cause acute disease in the young of multiple species, including humans, cattle, sheep, cats, dogs, deer, chickens, turkeys, and ducks (Bridger, 1980; Gough et al., 1984; Harboav et al., 1987; Madeley et al., 1975; McNulty et al., 1988; Snodgrass et al., 1977; Tzipon et al., 1981; Williams, 1980; Woode et al., 1978), and multiple serotypes have been described for human, bovine, and turkey astroviruses.
Astroviruses are commonly recognized as a problem in turkeys. Turkey astrovirus (TAstV) was first described by McNulty et al. (1980) in poults in the United Kingdom suffering from diarrhea and increased mortality. In the United States, TAstV was first identified in the 1980s (TAstV-1), and shown to be widely distributed (Reynolds et al., 1986; Reynolds et al., 1987b; Saif et al., 1985). Reynolds et al. (1987b) demonstrated that astroviruses could be isolated from 78% of diseased turkey flocks, more than any other virus identified. TAstV is generally associated with self-limiting mild enteritis, transient growth depression, moderate increases in mortality (Jonassen et al., 2003; Koci et al., 2000; McNulty et al., 1980; Reynolds, 1991; Reynolds et al., 1987b; Yu et al., 2000) and malabsorption (Reynolds et al., 1986; Reynolds et al., 1987a; Thouvenelle et al., 1995a; Thouvenelle et al., 1995b).
Recently, a TAstV isolate, TAsV-2, that is associated with poult enteritis and mortality syndrome (PEMS), was characterized (Koci et al., 2000). PEMS is a multifactorial, highly infectious emerging disease that affects young turkeys, typically between 7 and 28 days of age. The disease was first described in 1991 in an area along the western North Carolina/South Carolina border (Barnes et al., 1997). A PEMS-like disease has been described in most turkey producing states across the United States (Barnes et al., 1997; Brandenberger, 1999), and has been estimated to cost the turkey industry over $100 million (Brandenberger, 1999). TAstV-2 is genetically and immunologically distinct from previously described isolates (Koci et al., 2000).
Strict containment is the only known method of preventing and controlling infections with any of the known astroviruses. Infected flocks, especially those that exhibit severe loss in viability and production, need to be treated with the utmost concern for biosecurity, strictly adhering to the principles discussed in Zander & Mallinson (1991). Astroviruses are extremely stable in the environment and resistant to inactivation by most routinely used disinfectants (Kurtz et al., 1980; Abad et al., 1997; Schultz-Cherry et al., 2001) similar to chicken anemia virus or foot-and-mouth disease virus. For instance, partially purified TAstV-2 remains infectious following treatment with a panel of commercial disinfectants, including 10% bleach. TAstV-2 is also very heat stable, resisting inactivation following treatment at 60° C. for 10 minutes, and resistant to low pH (Schultz-Cherry et al., 2001). These findings suggest that, once a poultry production facility has been infected with astrovirus, complete sanitation of all materials and restricted access to facilities by personnel is required to contain the outbreak to an affected farm.
The combination of age susceptibility and highly stable virions suggests that multiple age farms may help prolong the period of poor production as older birds may recover and no longer exhibit clinical signs but still harbor virus. For example, new poults routinely develop enteritis soon after being placed in “cleaned” houses on farms with multiple aged birds (Edens & Doerfler, 1999). The most practical prevention method is to use strict biosecurity prophylactically. A nominal investment of time and energy spent on keeping each farm pathogen-free could greatly reduce the likelihood of contracting an astrovirus infection, and likewise periods of prolonged poor production.
Until recently the most common method to identify astrovirus infection in birds was electronmicroscopy (EM) (Reynolds, 1991). However, only 10% of particles may exhibit the 5- or 6-pointed starlike morphology making it difficult to accurately identify astroviruses using direct EM, especially when there are very few viral particles present (Caul & Appleton, 1982; Reynolds, 1991; Matsui & Greenberg, 2001). Because of this limitation, Reynolds (1991) suggested using immune EM (IEM) to encourage viral aggregation, however, the addition of purified antibody or convalescent sera to a virus sample can actually mask characteristic physical features or fail to detect new serotypes (Matsui & Greenberg, 2001).
Currently, the one diagnostic tool available for TAstV-2 is a reverse transcriptase-polymerase chain reaction (RT-PCR) assay (Koci et al., 2000). However, such assays require ongoing infection, and the results can be greatly affected by sampling methods. In addition, RT-PCR requires diagnostic facilities capable of performing molecular biology techniques, something many state diagnostic laboratories lack.
Thus, what is needed is an improved method to detect an animal exposed to an astrovirus, e.g., TAsV-2.